Abstract
Obesity, a chronic low-grade inflammatory condition is associated with the development of many comorbidities including dyslipidemia. This review examines interactions between single nucleotide polymorphisms (SNP) in the inflammatory genes tumor necrosis alpha (TNFA) and interleukin-6 (IL-6) and dietary fatty acids, and their relationship with obesity and serum lipid levels. In summary, dietary fatty acids, in particular saturated fatty acids and the omega-3 and omega-6 polyunsaturated fatty acids, impact the expression of the cytokine genes TNFA and IL-6, and alter TNFα and IL-6 production. In addition, sequence variants in these genes have also been shown to alter their gene expression and plasma levels, and are associated with obesity, measures of adiposity and serum lipid concentrations. When interactions between dietary fatty acids and TNFA and IL-6 SNPs on obesity and serum lipid were analyzed, both the quantity and quality of dietary fatty acids modulated the relationship between TNFA and IL-6 SNPs on obesity and serum lipid profiles, thereby impacting the association between phenotype and genotype. Researching these diet–gene interactions more extensively, and understanding the role of ethnicity as a confounder in these relationships, may contribute to a better understanding of the inter-individual variability in the obese phenotype.
Highlights
Obesity, a chronic low-grade inflammatory condition, is associated with the development of many comorbidities, including cardiovascular disease (CVD), type 2 diabetes, and a number of cancers [1]
This review suggests that DNA sequence variations in genes involved in inflammation may interact with environmental exposures, such as dietary intake, to modulate an individual’s susceptibility to developing obesity and its comorbidities
When interactions between dietary fatty acids with TNFA and IL-6 single nucleotide polymorphisms (SNP) on obesity and serum lipid were analyzed, it became evident that both the quantity and quality of dietary fatty acids modulate the relationship between TNFA and IL-6 SNPS on obesity and serum lipid profiles, thereby impacting the association between phenotype and genotype
Summary
A chronic low-grade inflammatory condition, is associated with the development of many comorbidities, including cardiovascular disease (CVD), type 2 diabetes, and a number of cancers [1]. Lifestyle factors, including dietary components, such as fatty acids, interact with genetic variants to regulate the development and progression of obesity and its comorbidities. These complex interactions may explain differences observed in the obese phenotype and its comorbidities that vary both within and across populations [3,4,5,6]. Functional polymorphisms have been reported in the TNFA, IL-1, IL-6 and lymphotoxin-α (LTA) inflammatory genes, altering cytokine production [17,18,19,20] These polymorphisms have been shown to interact with dietary fatty acids to regulate production and secretion of cytokines, predisposing an individual to inflammation and altering obesity and associated comorbidity risk [6,21]. It was shown that total plasma PUFA/SFA levels modified the observed additive genetic effects of IL-6, TNFA and LTA [23], highlighting the importance of studying nutrigenetic SNP-SNP or gene-gene interactions
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